Lead and Neurotoxicity

Sharma, Praveen; Chambial, Shailja; Shukla, Kamla Kant

doi:10.1007/s12291-015-0480-6

Cited by 59 publications

(32 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lead-induced neurotoxicity (LIN), a condition whose insidious effect could be unrecognised particularly in the early years, remains a topic of substantial concern and interest particularly in developing countries where about 99% of 600,000 new cases of children with intellectual disabilities as a result of lead exposure reside (WHO, 2013;Sharma et al, 2015). Thus, this study attempted to determine the possible role of the combination of blood lead level, intelligent quotient and erythrocyte acetylcholinesterase activity in the early detection of lead-induced neurotoxicity in Children.…”

Section: Discussionmentioning

confidence: 99%

“…Lead toxicity may be explained by its interference with the activity of the most enzymes. Lead could bind to the thiol-groups of these proteins or displace some essential metal ions that are necessary for their normal functioning (Sharma et al, 2015). However, the mechanism by which lead alters AChE activity is still incompletely understood as this enzyme does not contain free thiol groups in its structure to which Pb could bind (Rosenberry & Soggin, 1984;Ademuyiwa et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Positive and inverse correlation of blood lead level with erythrocyte acetylcholinesterase and intelligence quotient in children: implications for neurotoxicity

Nwobi

Adedapo

Olukolade

et al. 2019

Interdisciplinary Toxicology

View full text Add to dashboard Cite

Blood lead level (BLL) is insufficiently sensitive for early detection of Lead-induced neurotoxicity (LIN). This study determined the possible role of the combination of BLL, intelligent quotient (IQ) and erythrocyte acetylcholinesterase (AChE) activity in the early detection of LIN in Children. Apparently healthy children (n=309) from eight public primary schools in Ibadan, Nigeria were recruited and classified into: children with Elevated BLL (EBLL) and children with Acceptable BLL (control) based on CDC cut-off for childhood lead exposure. Neurological indices (speech, memory, cranial nerves and cerebellar functions), IQ, BLL and erythrocyte AChE activity were assessed using standard methods, Standard Progressive Matrices, AAS and HPLC respectively. Statistical analysis involved Student’s t-test, Pearson’s correlation and multivariate regression. p<0.05 was considered significant. There were 169 (54.7%) children with EBLL while there were 140 (45.3%) control children. Both groups exhibited normal speech, memory, cranial nerves and cerebellar functions. However, IQ was lower in EBLL children (85.9±11.6) compared with control (91.5±14.0) while BLL and AChE activity were higher in EBLL children (0.4±0.1 µmol/l; 117.5±25.5 µkat/l) compared with control (0.2±0.0 µmol/l; 59.4±10.2 µkat/l). BLL showed inverse correlation with IQ (r=–0.134, p=0.019) but positive correlation with AChE (r=0.978, p≤0.001). 16.2% of the observed variation in BLL could be accounted for by AChE using the equation; [BLL=–0.007+0.003 AChE] p<0.05. Elevated blood lead level is prevalent among the school children and appears to have adverse effect on their IQ. Erythrocyte AChE could be a promising marker for early recognition of significant environmental lead exposure and lead-induced neurotoxicity in children.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Positive and inverse correlation of blood lead level with erythrocyte acetylcholinesterase and intelligence quotient in children: implications for neurotoxicity

Nwobi

Adedapo

Olukolade

et al. 2019

Interdisciplinary Toxicology

View full text Add to dashboard Cite

show abstract

“…In the brain, Pb neurotoxicity is prominent in prefrontal cortex, hippocampus and cerebellum, 10 where it results in morphological, structural and pathological changes in neuronal cells and their synaptic connections. 8 , 59 , 60 Mecha nisms of lead neurotoxicity are complex.…”

Section: Discussionmentioning

confidence: 99%

“…While Pb affects virtually all organs and organ systems in the body including cardiovascular, renal and reproductive systems, 2 its ability to act as a potent and pervasive neurotoxin is well documented. 8 – 10 Pb is permeable to the blood–brain barrier, possibly through the action of Ca 2+ -ATPase, and rapidly accumulates in neurons and astrocytes. 11 In fact, the nervous system is regarded as among the most vulnerable target of Pb toxicity, which is evident by behavioral abnormalities, neuromuscular disabilities and cognitive deficits in events of Pb exposure.…”

Section: Introductionmentioning

confidence: 99%

Dysfunction of cortical synapse-specific mitochondria in developing rats exposed to lead and its amelioration by ascorbate supplementation

Ahmad¹,

Salahuddin²,

Alamoudi³

et al. 2018

NDT

View full text Add to dashboard Cite

BackgroundLead (Pb) is a widespread environmental neurotoxin and its exposure even in minute quantities can lead to compromised neuronal functions. A developing brain is particularly vulnerable to Pb mediated toxicity and early-life exposure leads to permanent alterations in brain development and neuronal signaling and plasticity, culminating into cognitive and behavioral dysfunctions and elevated risk of neuropsychiatric disorders later in life. Nevertheless, the underlying biochemical mechanisms have not been completely discerned.MethodsBecause of their ability to fulfill high energy needs and to act as calcium buffers in events of high intensity neuronal activity as well as their adaptive regulatory capability to match the requirements of the dynamicity of synaptic signaling, synapse-specific or synaptic mitochondria (SM) are critical for synaptic development, function and plasticity. Our aim for the present study hence was to characterize the effects of early-life Pb exposure on the functions of SM of prepubertal rats. For this purpose, employing a chronic model of Pb neurotoxicity, we exposed rat pups perinatally and postnatally to Pb and used a plethora of colorimetric and fluorometric assays for assessing redox and bioenergetic properties of SM. In addition, taking advantage of its ability as an antioxidant and as a metal chelator, we employed ascorbic acid (vitamin C) supplementation as an ameliorative therapeutic strategy against Pb-induced neurotoxicity and dysfunction of SM.ResultsOur results suggest that early-life exposure to Pb leads to elevated oxidative stress in cortical SM with consequent compromises in its energy metabolism activity. Ascorbate supplementation resulted in significant recovery of Pb-induced oxidative stress and functional compromise of SM.ConclusionAlterations in redox status and bioenergetic properties of SM could potentially contribute to the synaptic dysfunction observed in events of Pb neurotoxicity. Additionally, our study provides evidence for suitability of ascorbate as a significant ameliorative agent in tacking Pb neurotoxicity.

show abstract

“…Exposure to Pb, even in low doses, results in various adverse consequences, particularly in the brain [8]. Pb, as a neurotoxicant, crosses the blood-brain barrier to cause oxidative stress [9], morphologic damage, neurodegeneration and cognitive impairment in the brain, particularly that of developing brain [10][11][12][13]. The prefrontal cortex (PFC), which accounts for one-third of the human cerebral cortex, is responsible for working memory, higher reasoning, decision making and many other executive functions [14,15].…”

Section: Introductionmentioning

confidence: 99%

Lead acetate-induced neurodegenerative changes in the dorsolateral prefrontal cortex of mice: the role of Vitexin

Amedu

Omotoso

2020

Environ Anal Health Toxicol

View full text Add to dashboard Cite

This study was aimed at investigating the neuroprotective effect of Vitexin against lead (Pb) induced neurodegenerative changes in the dorsolateral prefrontal cortex (DLPFC) and working memory in mice. Thirty-two adolescent male albino mice were divided into four groups (n=8). Control group received 0.2 mL of normal saline; Pb group received 100 mg/kg of Pb acetate for 14 days, Vitexin group received 1mg/kg of Vitexin for 14 days, and Pb+Vitexin group received 100 mg/kg of Pb acetate and 1 mgkg of Vitexin for 14 days. Barnes maze test and novel object recognition test were done to ascertain working memory. Histoarchitectural assessment of DLPFC was done with haematoxylin and eosin (H&E), cresyl fast violet and congo red stains. Furthermore, cell count and other morphometric measurements were done. There was significant decline in working memory in the Pb group, but a combination of Pb+Vitexin improved the working memory. Vitexin significantly reduced neuronal death and chromatolysis caused by Pb. Amyloid aggregation was not observed in any of the groups. This study has shown that concurrent administration of Vitexin and Pb will significantly reduce neurodegeneration and improve working memory. However, Pb treatment or Pb+Vitexin treatment does not have any effect on intercellular distance, neuronal length and the cross-sectional area of neurons in layer III of DLPFC.

show abstract

Lead and Neurotoxicity

Cited by 59 publications

References 9 publications

Positive and inverse correlation of blood lead level with erythrocyte acetylcholinesterase and intelligence quotient in children: implications for neurotoxicity

Positive and inverse correlation of blood lead level with erythrocyte acetylcholinesterase and intelligence quotient in children: implications for neurotoxicity

Dysfunction of cortical synapse-specific mitochondria in developing rats exposed to lead and its amelioration by ascorbate supplementation

Lead acetate-induced neurodegenerative changes in the dorsolateral prefrontal cortex of mice: the role of Vitexin

Contact Info

Product

Resources

About